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Article: The Roles of Lipocalin-2 in Small-for-Size Fatty Liver Graft Injury

TitleThe Roles of Lipocalin-2 in Small-for-Size Fatty Liver Graft Injury
Authors
Issue Date2014
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.annalsofsurgery.com
Citation
Annals of Surgery, 2014, v. 260 n. 6, p. 1062-1072 How to Cite?
AbstractOBJECTIVE:: To investigate the roles and underlying mechanism of an inflammatory mediator-lipocalin-2 (Lcn2) in small-for-size fatty graft liver injury. BACKGROUND:: Understanding of the distinct mechanism regulating small-for-size fatty liver graft injury will be crucial to prevent marginal graft failure during living donor liver transplantation (LDLT). METHODS:: The roles of Lcn2 in small fatty graft injury were investigated in orthotopic liver transplantation model rats, human LDLT samples, an in vitro simulated ischemia-reperfusion (IR) model, and a hepatic ischemic reperfusion plus major hepatectomy (IR + H) model in mice. RESULTS:: Our result showed that Lcn2 was significantly upregulated together with elevation of chemokine (C-X-C motif) ligand 10 (CXCL10) and activation/infiltration of intragraft macrophages after liver transplantation using small-for-size fatty liver graft compared with that of using small-for-size normal liver graft. Intragraft and plasma levels of Lcn2 were intensified in patients who underwent transplantation with small-for-size fatty graft after LDLT. Lcn2 and CXCL10 were expressed higher in fatty hepatocytes after the simulated IR injury compared with normal hepatocytes. Overexpression of Lcn2 significantly deteriorated IR + H-induced hepatic injury in correlation with upregulation of CXCL10 and augmentation of infiltrated macrophages. On the contrary, hepatic injury of small fatty liver remnant after IR + H operation was attenuated in the Lcn-2 mice because of suppression of CXCL10 expression and diminishment of macrophage infiltration. CONCLUSIONS:: Lcn2 is an important regulator in small-for-size fatty liver graft injury and targeting Lcn2 may be feasible for preventing marginal graft failure in LDLT.
Persistent Identifierhttp://hdl.handle.net/10722/194716
ISSN
2015 Impact Factor: 8.569
2015 SCImago Journal Rankings: 4.503

 

DC FieldValueLanguage
dc.contributor.authorCheng, Q-
dc.contributor.authorNg, KTP-
dc.contributor.authorXu, A-
dc.contributor.authorLi, CX-
dc.contributor.authorLiu, XB-
dc.contributor.authorGuo, DY-
dc.contributor.authorPoon, RTP-
dc.contributor.authorFan, ST-
dc.contributor.authorLo, CM-
dc.contributor.authorMan, K-
dc.date.accessioned2014-02-17T02:04:40Z-
dc.date.available2014-02-17T02:04:40Z-
dc.date.issued2014-
dc.identifier.citationAnnals of Surgery, 2014, v. 260 n. 6, p. 1062-1072-
dc.identifier.issn0003-4932-
dc.identifier.urihttp://hdl.handle.net/10722/194716-
dc.description.abstractOBJECTIVE:: To investigate the roles and underlying mechanism of an inflammatory mediator-lipocalin-2 (Lcn2) in small-for-size fatty graft liver injury. BACKGROUND:: Understanding of the distinct mechanism regulating small-for-size fatty liver graft injury will be crucial to prevent marginal graft failure during living donor liver transplantation (LDLT). METHODS:: The roles of Lcn2 in small fatty graft injury were investigated in orthotopic liver transplantation model rats, human LDLT samples, an in vitro simulated ischemia-reperfusion (IR) model, and a hepatic ischemic reperfusion plus major hepatectomy (IR + H) model in mice. RESULTS:: Our result showed that Lcn2 was significantly upregulated together with elevation of chemokine (C-X-C motif) ligand 10 (CXCL10) and activation/infiltration of intragraft macrophages after liver transplantation using small-for-size fatty liver graft compared with that of using small-for-size normal liver graft. Intragraft and plasma levels of Lcn2 were intensified in patients who underwent transplantation with small-for-size fatty graft after LDLT. Lcn2 and CXCL10 were expressed higher in fatty hepatocytes after the simulated IR injury compared with normal hepatocytes. Overexpression of Lcn2 significantly deteriorated IR + H-induced hepatic injury in correlation with upregulation of CXCL10 and augmentation of infiltrated macrophages. On the contrary, hepatic injury of small fatty liver remnant after IR + H operation was attenuated in the Lcn-2 mice because of suppression of CXCL10 expression and diminishment of macrophage infiltration. CONCLUSIONS:: Lcn2 is an important regulator in small-for-size fatty liver graft injury and targeting Lcn2 may be feasible for preventing marginal graft failure in LDLT.-
dc.languageeng-
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.annalsofsurgery.com-
dc.relation.ispartofAnnals of Surgery-
dc.rightsThis is a non-final version of an article published in final form in Annals of Surgery, 2014, v. 260 n. 6, p. 1062-1072-
dc.titleThe Roles of Lipocalin-2 in Small-for-Size Fatty Liver Graft Injury-
dc.typeArticle-
dc.identifier.emailNg, KTP: ledodes@hku.hk-
dc.identifier.emailXu, A: amxu@hkucc.hku.hk-
dc.identifier.emailLi, CX: doclicx@hku.hk-
dc.identifier.emailLiu, XB: liuxb301@hku.hk-
dc.identifier.emailPoon, RTP: poontp@hku.hk-
dc.identifier.emailFan, ST: stfan@hku.hk-
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hk-
dc.identifier.emailMan, K: kwanman@hku.hk-
dc.identifier.authorityNg, KTP=rp01720-
dc.identifier.authorityXu, A=rp00485-
dc.identifier.authorityPoon, RTP=rp00446-
dc.identifier.authorityFan, ST=rp00355-
dc.identifier.authorityLo, CM=rp00412-
dc.identifier.authorityMan, K=rp00417-
dc.identifier.doi10.1097/SLA.0000000000000427-
dc.identifier.pmid24374540-
dc.identifier.hkuros227962-
dc.identifier.hkuros228569-
dc.identifier.hkuros246924-
dc.identifier.volume260-
dc.identifier.issue6-
dc.identifier.spage1062-
dc.identifier.epage1072-
dc.publisher.placeUnited States-

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